Following the cloning and sequencing of the cellular TNF receptors in the early 1990s, it was noticed that several virus genes in the database shared remarkable sequence similarity to the external cysteine-rich domain (CRD) repeat sequences that comprised the binding sites for TNF. Unlike the cellular receptors, however, the viral versions were predicted to be secreted glycoproteins that could scavenge host TNF prior to binding with its cognate cellular receptors. These viral genes, first identified in several poxviruses, were the first documented examples of bviroceptors\ or virus-encoded receptor homologs that function to bind and sequester cellular ligands away from the appropriate cellular receptors.